The research is directed toward various questions of kidney function. One aspect concerns the effect of sodium transport inhibitors on adenine nucleotide levels. The rate of utilization and regeneration of ATP determine its steady-state level. The turnover rate of ATP in the kidney is very rapid, and interference with ATP metabolism is easily detected by measuring tissue levels of this nucleotide. Ouabain has been known for some time to be an inhibitor of a particular enzyme system that utilizes ATP, and, in theory, if ouabain acts in vivo to inhibit this enzyme, the ATP level should rise. We have found in the perfused kidney that ouabain is an effective inhibitor of sodium reabsorption, and that the tissue ATP level is raised by approximately 25% (from about 6.2 umol/g, wet weight) in ouabain-treated kidneys. Furosemide, on the other hand, inhibits sodium reabsorption without altering ATP levels. Together with other information, we interpret these results as supporting the hypothesis that furosemide does not inhibit sodium transport by the same mechanism as does ouabain. Metabolism and fate of adenosine 3', 5'-monophosphate (cyclic AMP) within the kidney. This is a major area of our research. Summarized data to date are that exogenous cyclic AMP is rapidly taken up by the kidney, both in vivo and in vitro. The products of the cyclic AMP metabolism are ATP, ADP, and uric acid. The uric acid (about one-half of the total metabolic products) leaves the kidney and enters the plasma or the urine.